Interleukin-13 increases prostaglandin E2 (PGE2) production by normal human polymorphonuclear neutrophils by enhancing cyclooxygenase 2 (COX-2) gene expression

1998 ◽  
Vol 47 (4) ◽  
pp. 167-173 ◽  
Author(s):  
C.-L. Yu ◽  
M.-H. Huang ◽  
Y.-Y. Kung ◽  
C.-Y. Tsai ◽  
Y.-Y. Tsai ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostaglandin E2 ◽  
Cyclooxygenase 2 ◽  
Pge2 Production ◽  
Polymorphonuclear Neutrophils ◽  
Interleukin 13 ◽  
Normal Human ◽  
Cox 2

scholarly journals Induction of Cyclooxygenase-2 Gene in Pancreatic β-Cells by 12-Lipoxygenase Pathway Product 12-Hydroxyeicosatetraenoic Acid

2002 ◽  
Vol 16 (9) ◽  
pp. 2145-2154 ◽  
Author(s):  
Xiao Han ◽  
Songyuan Chen ◽  
Yujie Sun ◽  
Jerry L. Nadler ◽  
David Bleich
Keyword(s):  
Gene Expression ◽  
Prostaglandin E2 ◽  
Cyclooxygenase 2 ◽  
Pge2 Production ◽  
Hydroxyeicosatetraenoic Acid ◽  
Lipoxygenase Inhibitor ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Cox 2 ◽  
12 Lipoxygenase

Abstract Cyclooxygenase-2 (COX-2) gene and 12-lipoxygenase (12-LO) gene are preferentially expressed over other types of cyclooxygenase and lipoxygenase in pancreatic β-cells. Inhibition of either COX-2 or 12-LO can prevent cytokine-induced pancreatic β-cell dysfunction as defined by inhibition of glucose-stimulated insulin secretion. As cellular stress induces both genes and their respective end products in pancreatic β-cells, we evaluated the role of 12-hydroxyeicosatetraenoic acid (HETE) on COX-2 gene expression, protein expression, and prostaglandin E2 (PGE2) production. We demonstrate that 12-HETE significantly increases COX-2 gene expression and consequent product formation, whereas a closely related lipid, 15-HETE, does not. In addition, IL-1β-stimulated prostaglandin E2 production is completely inhibited by a preferential lipoxygenase inhibitor cinnaminyl-3,4-dihydroxy-α-cyanocinnamate. We then evaluated IL-1β-induced PGE2 production in islets purified from control C57BL/6 mice and 12-LO knockout mice lacking cytokine-inducible 12-HETE. IL-1β stimulated an 8-fold increase in PGE2 production in C57BL/6 islets but failed to stimulate PGE2 in 12-LO knockout islets. Addition of 12-HETE to 12-LO knockout islet cells produced a statistically significant rise in PGE2 production. Furthermore, 12-HETE, but not 15-HETE, stimulated COX-2 promoter and activator protein-1 binding activity. These data demonstrate that 12-HETE mediates cytokine-induced COX-2 gene transcription and resultant PGE2 production in pancreatic β-cells.

scholarly journals Marine Alga Ecklonia cava Extract and Dieckol Attenuate Prostaglandin E2 Production in HaCaT Keratinocytes Exposed to Airborne Particulate Matter

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 190 ◽  
Author(s):  
Jae Won Ha ◽  
Hyerim Song ◽  
Seong Su Hong ◽  
Yong Chool Boo
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Particulate Matter ◽  
Prostaglandin E2 ◽  
Pge2 Production ◽  
Ecklonia Cava ◽  
Epidermal Keratinocytes ◽  
Hacat Keratinocytes ◽  
Cox 2 ◽  
Cox 1

Atmospheric particulate matter (PM) is an important cause of skin damage, and an increasing number of studies have been conducted to discover safe, natural materials that can alleviate the oxidative stress and inflammation caused by PM. It has been previously shown that the extract of Ecklonia cava Kjellman, a perennial brown macroalga, can alleviate oxidative stress in epidermal keratinocytes exposed to PM less than 10 microns in diameter (PM10). The present study was undertaken to further examine the anti-inflammatory effects of E. cava extract and its major polyphenolic constituent, dieckol. HaCaT keratinocytes were exposed to PM10 in the presence or absence of E. cava extract or dieckol and analyzed for their viability, prostaglandin E2 (PGE2) release, and gene expression of cyclooxygenase (COX)-1, COX-2, microsomal prostaglandin E2 synthase (mPGES)-1, mPGES-2, and cytosolic prostaglandin E2 synthase (cPGES). PM10 treatment decreased cell viability and increased the production of PGE2, and these changes were partially abrogated by E. cava extract. E. cava extract also attenuated the expression of COX-1, COX-2, and mPGES-2 stimulated by PM10. Dieckol attenuated PGE2 production and the gene expression of COX-1, COX-2, and mPGES-1 stimulated by PM10. This study demonstrates that E. cava extract and dieckol alleviate airborne PM10-induced PGE2 production in keratinocytes through the inhibition of gene expression of COX-1, COX-2, mPGES-1, and/or mPGES-2. Thus, E. cava extract and dieckol are potentially useful natural cosmetic ingredients for counteracting the pro-inflammatory effects of airborne PM.

Mikroglia und immunologische Mechanismen in der neuropsychiatrischen Forschung

2014 ◽  
Vol 33 (11) ◽  
pp. 761-770
Author(s):  
M. J. Schwarz ◽  
B. Leitner ◽  
E. Weidinger ◽  
N. Müller
Keyword(s):  
Prostaglandin E2 ◽  
Cyclooxygenase 2 ◽  
Cox 2

ZusammenfassungDie Psychoneuroimmunologie beschäftigt sich mit den Wechselwirkungen zwischen der (gesunden) Psyche, psychischen Störungen und dem Immunsystem. Inzwischen hat sich gezeigt, dass zumindest bei Subgruppen psychischer Störungen wie Schizophrenie und Depression ein entzündlicher Prozess bei der Pathogenese eine Rolle spielt. Da für Schizophrenie und Depression auf diesem Gebiet die meisten Befunde vorliegen, konzentriert sich diese Übersicht auf diese beiden Störungsbilder. Die differenzielle Aktivierung von Mikrogliazellen und Astrozyten als funktionelle Träger des Immunsystems im ZNS, trägt zur Typ-1/Typ-2-Inbalance bei. Das entzündliche Geschehen ist verbunden mit höherer Prostaglandin-E2 (PGE-2)-Produktion und erhöhter Cyclooxygenase-2 (COX-2)-Expression. Zunehmende Evidenz aus klinischen Studien mit COX-2-Inhibitoren weisen auf einen günstigen Effekt antiinflammatorischer Therapie bei Schizophrenie hin, speziell in frühen Stadien der Krankheit. Sowohl bei Depression als auch bei Schizophrenie ist die Vulnerabilitäts- Stress-Hypothese weitgehend akzeptiert. So zeigte sich z. B. dass – bei entsprechender genetischer Disposition – Stress im frühen Lebensalter oder Separationsstress mit einem Anstieg proinflammatorischer Zytokine einhergehen und zu einer Immunaktivierung führen. Die Interaktionen zwischen dem Immunsystem, Neurotransmittern und dem Tryptophan- Kynurenin-System sind entscheidende Komponenten für die Pathogenese von Stress und Depression. Eine antientzündliche Behandlung, z. B. mit dem COX-2-Inhibitor Celecoxib, zeigt antidepressive Effekte.

scholarly journals Expression Profiles of the Progesterone Receptor, Cyclooxygenase-2, Growth Differentiation Factor 9, and Bone Morphogenetic Protein 15 Transcripts in the Canine Oviducts during the Oestrous Cycle

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 454
Author(s):  
Jaime Palomino ◽  
Javiera Flores ◽  
Georges Ramirez ◽  
Victor H. Parraguez ◽  
Monica De los Reyes
Keyword(s):  
Gene Expression ◽  
Bone Morphogenetic Protein ◽  
Cyclooxygenase 2 ◽  
Oestrous Cycle ◽  
Progesterone Concentration ◽  
Plasma Progesterone ◽  
Morphogenetic Protein ◽  
Growth Differentiation Factor 9 ◽  
Bone Morphogenetic Protein 15 ◽  
Cox 2

The gene expression in the canine oviduct, where oocyte maturation, fertilization, and early embryonic development occur, is still elusive. This study determined the oviductal expression of (PR), cyclooxygenase-2 (COX-2), growth differentiation factor 9 (GDF-9), and bone morphogenetic protein 15 (BMP-15) during the canine oestrous cycle. Samples were collected from bitches at anoestrus (9), proestrus (7), oestrus (8), and dioestrus (11), after routine ovariohysterectomy and the ovarian surface structures and plasma progesterone concentration evaluated the physiological status of each donor. The oviductal cells were isolated and pooled. Total RNA was isolated, and gene expression was assessed by qPCR followed by analysis using the t-test and ANOVA. The PR mRNA increased (P < 0.05) from the anoestrus to dioestrus with the plasma progesterone concentration (r = 0.8). COX-2 mRNA expression was low in the anoestrus and proestrus, and negligible in the oestrus, while it was around 10-fold higher (P < 0.05) in the dioestrus. The GDF-9 mRNA was expressed during all phases of the oestrous cycle and was most abundant (P < 0.05) during oestrus phase. The BMP-15 mRNA decreased (P < 0.05) in the anoestrus and proestrus phases. Thus, the transcripts were differentially expressed in a stage-dependent manner, suggesting the importance of oestrous cycle regulation for successful reproduction in dogs.

Regulation of macrophage cyclooxygenase-2 gene expression by modifications of histone H3

2004 ◽  
Vol 286 (5) ◽  
pp. L956-L962 ◽  
Author(s):  
Gye Young Park ◽  
Myungsoo Joo ◽  
Tetyana Pedchenko ◽  
Timothy S. Blackwell ◽  
John W. Christman
Keyword(s):  
Gene Expression ◽  
Chromatin Structure ◽  
Gene Activation ◽  
Histone H3 ◽  
Major Effect ◽  
Cyclooxygenase 2 ◽  
Raw 264.7 Cells ◽  
Transcriptional Level ◽  
Sequence Motif ◽  
Cox 2

Some transcription factors involved in the regulation of cyclooxygenase 2 (COX-2) expression in macrophage, including NF-κB, interact with p300, which contains histone acetyltransferase (HAT) enzyme complex. Chromatin structure is regulated by modifying enzymes, including HAT, and plays an important role in eukaryotic gene regulation through histone modification. We hypothesized that changes in chromatin structure related to phosphorylation and acetylation of histone H3 adjacent to key DNA binding sequence motif in the COX-2 promoter contribute to COX-2 gene activation in macrophages. Sodium butyrate (NaBT) is a short-chain fatty acid that possesses histone deacetyltransferase-inhibiting activity. Our data show that NaBT accentuates LPS-induced COX-2 gene expression at a transcriptional level, even though NaBT alone does not induce the COX-2 gene expression. Using a chromatin immunoprecipitation assay, we showed that costimulation of RAW 264.7 cells with NaBT and LPS synergistically increases COX-2 gene expression through both acetylation and phosphorylation of histone H3 at the promoter site. Our data show that NaBT accentuates LPS-induced COX-2 gene expression through MAP kinase-dependent increase of phosphorylation and acetylation of histone H3 at the COX-2 promoter site. These data indicate that posttranslational modification of histone H3 has a major effect on COX-2 gene expression by macrophages.

scholarly journals ApoL1 renal risk variants induce aberrant THP-1 monocyte differentiation and increase eicosanoid production via enhanced expression of cyclooxygenase-2

2018 ◽  
Vol 315 (1) ◽  
pp. F140-F150 ◽  
Author(s):  
Hewang Lee ◽  
Hila Roshanravan ◽  
Ying Wang ◽  
Koji Okamoto ◽  
Junghwa Ryu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Specific Inhibitor ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Monocyte Differentiation ◽  
Eicosanoid Production ◽  
Gene And Protein Expression ◽  
Cox 2 ◽  
Tgf Β1

Apolipoprotein L1 ( ApoL1) genetic variants are strongly associated with kidney diseases. We investigated the role of ApoL1 variants in monocyte differentiation and eicosanoid production in macrophages, as activated tissue macrophages in kidney might contribute to kidney injury. In human monocyte THP-1 cells, transient overexpression of ApoL1 (G0, G1, G2) by transfection resulted in a 5- to 11-fold increase in CD14 and CD68 gene expression, similar to that seen with phorbol-12-myristate acetate treatment. All ApoL1 variants caused monocytes to differentiate into atypical M1 macrophages with marked increase in M1 markers CD80, TNF, IL1B, and IL6 and modest increase in the M2 marker CD163 compared with control cells. ApoL1-G1 transfection induced additional CD206 and TGFB1 expression, and ApoL1-G2 transfection induced additional CD204 and TGFB1 expression. Gene expression of prostaglandin E2 (PGE2) synthase and thromboxane synthase and both gene and protein expression of cyclooxygenase-2 (COX-2) were increased by ApoL1-G1 and -G2 variants compared with -G0 transfection. Higher levels of PGE2 and thromboxane B2, a stable metabolite of thromboxane A2, and transforming growth factor (TGF)-β1 were released into the supernatant of cultured THP-1 cells transfected with ApoL1-G1 and -G2, but not -G0. The increase in PGE2, thromboxane B2, and TGF-β1 was inhibited by COX-2-specific inhibitor CAY10404 but not by COX-1-specific inhibitor SC-560. These results demonstrate a novel role of ApoL1 variants in the regulation of monocyte differentiation and eicosanoid metabolism, which could modify the immune response and promote inflammatory signaling within the local targeted organs and tissues including the kidney.

scholarly journals Selective Cyclooxygenase-2 Inhibition Impairs Glomerular Capillary Healing in Experimental Glomerulonephritis

2002 ◽  
Vol 13 (5) ◽  
pp. 1261-1270 ◽  
Author(s):  
Masashi Kitahara ◽  
Frank Eitner ◽  
Tammo Ostendorf ◽  
Uta Kunter ◽  
Ulf Janssen ◽  
...  
Keyword(s):  
Mesangial Cells ◽  
Healing Process ◽  
Cyclooxygenase 2 ◽  
Polymorphonuclear Neutrophils ◽  
Glomerular Injury ◽  
Systemic Hemodynamic ◽  
Glomerular Diseases ◽  
Glomerular Capillary ◽  
Cox 2 ◽  
Cox 2 Inhibitors

ABSTRACT. Selective cyclooxygenase-2 (COX-2) inhibitors have anti-inflammatory activity and reduce proteinuria in experimental membranous glomerulonephritis. Antiangiogenic properties of COX-2 inhibitors were recently reported. Whether these properties are relevant to the glomerular healing process in inflammatory glomerular diseases was investigated. For evaluation of the effects of selective COX-2 inhibitors on the glomerular healing process in a rat model of mesangioproliferative glomerulonephritis (induced by anti-Thy 1.1 antibody), a selective COX-2 inhibitor (rofecoxib or celecoxib) or vehicle was administered daily from day 1 after disease induction until euthanasia on day 6. Additional nephritic rats were treated with rofecoxib or vehicle from day 1 to day 10 and were monitored until day 28. Selective COX-2 inhibition led to significant increases in mesangiolysis (up to +71%) on days 2 and 6 and in albuminuria (up to 3.1-fold) on day 6. This augmentation of glomerular capillary damage was associated with rarefaction of glomerular endothelial cells, whereas the proliferation and activation of mesangial cells were not affected. No significant effects on the glomerular influx of polymorphonuclear neutrophils or the infiltration and proliferation of monocytes/macrophages at day 2 were noted. These effects were independent of systemic hemodynamic features, because rofecoxib did not affect systolic BP on day 2 or 5. Nephritic rats treated with rofecoxib for 10 d demonstrated persistent glomerular injury at day 28, as indicated by increased albuminuria (10-fold) and mesangial type IV collagen deposition (+24%). In normal rats, 5-d administration of rofecoxib failed to induce albuminuria or morphologic renal damage. In conclusion, selective COX-2 inhibitors impair glomerular capillary repair after mesangiolysis in rats with anti-Thy 1.1 glomerulonephritis. These data suggest that selective COX-2 inhibitors should be used with caution among patients with inflammatory endocapillary glomerular disorders.

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